Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Opioid substances act, both in the central and peripheral nervous systems, by regulating--via a specific receptor of the mu, delta or kappa type and a G protein--the activity of either of three recognized cellular effectors: adenylate cyclase, a K+ channel and a Ca++ channel. In the short term, opioid effects are of a neuromodulatory origin: they are likely to reflect opioid inhibition of neurotransmitter release (e.g.: of substance P in the spinal cord). In the long term, opioids induce the two adaptative phenomena known as tolerance and dependence whose mechanisms are considerably less well understood. Tolerance refers to a decreased responsiveness to the opioid upon repeated administration of the drug. Tolerance might reflect desensitization, a process which involves uncoupling of opioid receptor and of G protein (in the case of homologous desensitization) and, possibly, down-regulation of a G protein which the opioid receptor shares with other types of receptor (heterologous desensitization). Dependence refers to a latent, opioid-induced physiological state which expresses itself as a typical excitation syndrome upon withdrawal of the drug or administration of an opioid antagonist. The molecular events whereby dependence develops are unknown, yet they may involve (i) adenylate cyclase supersensitivity, an adaptation reaction where upon withdrawal of the inhibitory opioid induces an enhanced activity of the enzyme and, (ii) increased release of neurotransmitter (presynaptic facilitation).
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PMID:[Opioid receptors, tolerance and dependence]. 133 39